This invention relates generally to antiviral agents, and more particularly concerns an antiviral agent, which when mixed with a solvent carrier agent, is effective to abate herpes simplex virus disease (commonly referred to as herpes) and other related viral diseases.
Herpes simplex virus disease as its name indicates is the result of the infection of the human body by the herpes simplex virus. The herpes simplex virus that affects humans is of two types, type 1 and type 2. Both types of herpes simplex virus infect the human body by penetrating the cellular wall of the body cells and interfering with the DNA configuration of the cells. The herpes simplex virus takes over the DNA mechanism of the cell so that the virus can replicate itself. In the process of the herpes virus replicating itself within the cell, the cell is destroyed. As a result of the destruction of body cells a blister-like sore appears at the location where the herpes virus entered the body.
The type 1 herpes simplex virus is generally acknowledged to produce the characteristic blister-like sores at the mucocutaneous junctions at the mouth, nose and eyes. The type 2 herpes simplex virus is generally acknowledged to create the same sort of blister-like sores on the genitals and anus. The sores can appear, however, at any location on the body such as a wound, where the virus can enter the body.
It is also commonly acknowledged that once the virus has entered the human body it never leaves. After the blister-like sores have healed in about two to three weeks, the herpes virus retreats to and lies dormant in the nerve tissue of the body. Herpes simplex virus from oral herpes sequesters in the trigeminial ganglion, and in genital herpes in the sacral ganglion. As a result, some people experience recurring blister-like sores which are thought to be brought on by stress or other unknown triggering mechanisms within the body. In other people, the virus may lie dormant for long periods of time or for the rest of the person's life.
For those people, however, that experience frequent recurring blister-like sores, especially those with genital herpes, the disease can be especially traumatic. While there are a number of antiviral agents which will destroy the herpes simplex virus in a laboratory setting, none of these antiviral agents have been successful in combating oral or genital herpes simplex virus disease in a clinical setting. These antiviral agents include adenine arabinoside (ara-A), ribavirin, acyclovir (ACV), 2-deoxy-d-glucose (DG) and phosphonacetic acid (PAA). R. Hamilton, The Herpes Book, pages 161-168, (J. P. Tarcher, Inc., 1980); F. E. Kahn, Ed., Vol. 27, Antiobiotics and Chemotherapy, (Harper, Basel, 1980); and W. M. Shannon and F. M. Sachael, Jr., Vol. II, Pharmacology and Therapeutics, pages 263-390, (Pergamon Press, Ltd., 1980).
At the present time, the Federal Food and Drug Administration (FDA) has approved the use of ara-A in ointment form for treatment of ocular herpes simplex virus disease. Moreover, ara-A has also been used in the treatment of herpes encephalitis by infusing a solution of ara-A in sterile infusion fluid for 12 to 24 hours. Neither of these treatments are effective against oral or genital herpes. "Vidarabine Ophalthalmic Ointment (Vira-A)", Drug Therapy Bulletin, May 25, 1979, 17(11), pages 43-44; and "Vidarbine Approval for Herpes Simplex Virus Encephalitis", FDA Drug Bulletin, Dec. 1978 Jan. 1979, 8(6) 36.
Also at the present time, the Burroughs Wellcome Company of Research Triangle Park, N.C., has offered for sale an ointment under the trademark Zovirax, the active antiviral agent of which is acyclovir. The acyclovir antiviral agent in the Zovirax ointment is mixed with a polyethylene glycol base. Burroughs Wellcome's own literature and advertising state that "in studies of recurrent herpes genitalis and herpes labialis in nonimmunocompromised patients, there was no evidence of clinical benefit . . ."
The antiviral agent IdU (5-iododexyuridine) has been combined with dimethyl sulfoxide (DMSO) and has purportedly cleared up skin lesions caused by DNA viruses, including herpes simplex and prevent recurrence. F. O. MacCallum and B. E. Juel-Jensen, British Medical Journal, 2 pages 805-807, (1966); B. C. Turnbull and H. C. W. Stringer, New Zealand Medical Journal, 70, pages 317-320, (1969); and B. E. Juel-Jensen, F. O. MacCallum, A. M. R. Mackenzie and M. C. Pike, British Medical Journal, 4 pages 776-780 (1970). P. McGrady, The Persecuted Drug: The Story of DMSO, page 285, Grosset & Dunlap Co., 1973 (1981).
The apparent problem in abating or curing herpes simplex virus disease in a clinical setting results from the difficulty of assuring that the antiviral agent penetrates the cellular wall into the infrastructure of the cell in order to attack and kill the herpes simplex virus that are literally hiding behind the cellular wall structure.